Gut blood flow in fish during exercise and severe hypercapnia

This paper reviews the effects of exercise and hypercapnia on blood flow to the splanchnic circulation. Brief struggling behaviours are known to decrease blood flow to the gut (GBF). Likewise, prolonged swimming in unfed fish has been shown to reduce GBF in proportion to the increased oxygen uptake. Therefore, the normal postprandial increase in GBF theoretically should be impaired whenever fish are active. However, indirect evidence suggests that GBF is spared to some degree when fed fish swim continuously but at a cost (10-15%) to their critical swimming speed. Severe respiratory acidosis can be created by the new intensive aquaculture settings that use oxygen injection into re-circulated water. The only study so far to examine the effects of severe hypercapnia on GBF and its regulation showed that routine GBF and alpha-adrenergic control of GBF remained normal in unfed white sturgeon (Acipenser transmontanus). However, severe hypercapnia produced a hyperactive state and increased sensitivity of GBF to struggling. As a result, routine GBF was maintained for a short period of time. Thus, environmental changes such as severe hypercapnia can indirectly impact GBF through altered struggling behaviour, but the implications of the overall reduction in GBF to food assimilation have yet to be established.     

Gas-blood PCO2 gradients during avian gas exchange.

The avian respiratory system is a crosscurrent gas exchange system. One of the aspects of this type of gas exchange system is that end-expired PCO2 is greater than arterial PCO2, the highest possible value being equal to mixed venous PCO2. We made steady-state measurements of arterial, mixed venous, and end-expired PCO2 in anesthetized, spontaneously breathing chickens during inhalation of room air or 4-8% CO2. We found end-expired PCO2 to be higher than both arterial and mixed venous PCO2, the sign of the differences being such as to oppose passive diffusion. The observation that end-expired PCO2 was higher than arterial PCO2 can be explained on the basis of crosscurrent gas exchange. However, the observation that end-expired PCO2 exceeded mixed venous PCO2 must be accounted for by some other mechanism. The positive end-expired to mixed venous PCO2 gradients can be explained if it is postulated that the charged membrane mechanism suggested by Gurtner et al. (Respiration Physiol. 7: 173-187, 1969) is present in the avian lung.     

Regulation of arterial PCO2 during intravenous CO2 loading.

Increased CO2 flow to the lung produced by increasing cardiac output (with constant PVCO2) results in hyperpnea with arterial PCO2 maintained at its control value (J. Appl. Physiol. 36: 457, 1974). To study if arterial PCO2 could be similarly regulated when CO2 flow was elevated by increasing PVCO2 (without changing cardiac output), we produced graded increases in PVCO2 (up to a mean of 69 mmHg) using an extracorporeal gas exchanger in five chloralose-urethan-anesthetized dogs. CO2 output increased up to fourfold. Ventilation increased in proportion to the additional CO2 flow to the lung with consequent regulation of arterial PCO2 at its control value. Comparable increases in VE produced by "conventional" airway loading resulted in arterial hypercapnia. The resulting CO2 response curve was similar to that found in unanesthetized dogs. We conclude that intravenous delivery of CO2 to the lung results in infinite "sensitivity" when computed as Delta VE/Delta paco2. These results provide evidence for a CO2-linked hyperpnea which is not mediated by measurable increases in mean arterial PCO2.     

Ventral medullary extracellular fluid pH and PCO2 during hypoxemia

We designed experiments to study changes in ventral medullary extracellular fluid (ECF) PCO2 and pH during hypoxemia. Measurements were made in chloralose-urethan-anesthetized spontaneously breathing cats (n = 12) with peripherial chemodenervation. Steady-state measurements were made during normoxemia [arterial PO2 (PaO2) = 106 Torr], hypoxemia (PaO2 = 46 Torr), and recovery (PaO2 = 105 Torr), with relatively constant arterial PCO2 (approximately 44 Torr). Mean values of ventilation were 945, 683, and 1,037 ml/min during normoxemia, hypoxemia, and recovery from hypoxemia, respectively. Ventilatory depression occurred in each cat during hypoxemia. Mean values of medullary ECF PCO2 were 57.7 +/- 7.2 (SD), 59.4 +/- 9.7, and 57.4 +/- 7.2 Torr during normoxemia, hypoxemia, and recovery to normoxemia, respectively; respective values for ECF [H+] were 60.9 +/- 8.0, 64.4 +/- 11.6, and 62.9 +/- 9.2 neq/l. Mean values of calculated ECF [HCO3-] were 22.8 +/- 3.0, 21.7 +/- 3.3, and 21.4 +/- 3.1 meq/l during normoxemia, hypoxemia, and recovery, respectively. Changes in medullary ECF PCO2 and [H+] were not statistically significant. Therefore hypoxemia caused ventilatory depression independent of changes in ECF acid-base variables. Furthermore, on return to normoxemia, ventilation rose considerably, still independent of changes in ECF PCO2, [H+], and [HCO3-].     

Metabolic component of intestinal PCO(2) during dysoxia.

The adequacy of intestinal perfusion during shock and resuscitation might be estimated from intestinal tissue acid-base balance. We examined this idea from the perspective of conventional blood acid-base physicochemistry. As the O(2) supply diminishes with failing blood flow, tissue acid-base changes are first "respiratory, " with CO(2) coming from combustion of fuel and stagnating in the decreasing blood flow. When the O(2) supply decreases to critical, the changes become "metabolic" due to lactic acid. In blood, the respiratory vs. metabolic distinction is conventionally made using the buffer base principle, in which buffer base is the sum of HCO(3)(-) and noncarbonate buffer anion (A(-)). During purely respiratory acidosis, buffer base stays constant because HCO(3)(-) cannot buffer its own progenitor, carbonic acid, so that the rise of HCO(3)(-) equals the fall of A(-). During anaerobic "metabolism," however, lactate's H(+) is buffered by both A(-) and HCO(3)(-), causing buffer base to decrease. We quantified the partitioning of lactate's H(+) between HCO(3)(-) and A(-) buffer in anoxic intestine by compressing intestinal segments of anesthetized swine into a steel pipe and measuring PCO(2) and lactate at 5- to 10-min intervals. Their rises followed first-order kinetics, yielding k = 0. 031 min(-1) and half time = approximately 22 min. PCO(2) vs. lactate relations were linear. Over 3 h, lactate increased by 31 +/- 3 mmol/l tissue fluid (mM) and PCO(2) by approximately 17 mM, meaning that one-half of lactate's H(+) was buffered by tissue HCO(3)(-) and one-half by A(-). The data were consistent with a lumped pK(a) value near 6.1 and total A(-) concentration of approximately 30 mmol/kg. We conclude that the respiratory vs. metabolic distinction could be made in tissue by estimating tissue buffer base from measured pH and PCO(2).     

Esophageal PCO2 as a monitor of perfusion failure during hemorrhagic shock

Sato, Yoji, Max Harry Weil, Wanchun Tang, Shijie Sun,Jianlin Xie, Joe Bisera, and Hidehiro Hosaka. EsophagealPCO₂ as a monitor of perfusionfailure during hemorrhagic shock. J. Appl.Physiol. 82(2): 558-562, 1997.Measurement ofgastric wall PCO₂(Pg_CO2) bytonometric method has emerged as an attractive option for estimatingvisceral perfusion during circulatory shock. However, gastric acidsecretion obfuscates the tonometric measurement. We, therefore,investigated the option of measuringPCO₂ in the esophagus to minimizethese restraints. Hemorrhagic shock was induced in five Sprague-Dawleyrats, and five rats served as sham controls.Pg_CO2 wasmeasured with an ion-sensitive field effect transistor that wassurgically implanted into the gastric wall. Esophageal luminalPCO₂(Pe_CO2) wasmeasured by a second ion-sensitive field effect transistor sensor.During hemorrhagic shock, mean aortic pressure declined from 150 to 50 mmHg. Gastric blood flow decreased from 58 to 12 ml ^· min^{1 ·} 100 g¹ (21% of preshock) andesophageal blood flow from 44 to 7 ml ^· min^{1 ·} 100 g¹ (16% of preshock).Pg_CO2simultaneously increased from 47 to 116 Torr andPe_CO2 from 47 to 127 Torr. The increases inPg_CO2 werehighly correlated with increases inPe_CO2(r = 0.90). Esophageal tonometry may,therefore, serve as a practical alternative to gastric tonometry.

     

Effect of reducing anatomic dead space on arterial PCO2 during CO2 inhalation

Carotid body-denervated (CBD) ponies have a less than normal increase in arterial PCO2 (PaCO2) when inspired CO2 (PICO2) is increased, even when pulmonary ventilation (VE) and breathing frequency (f) are normal. We studied six tracheostomized ponies to determine whether this change 1) might be due to increased alveolar ventilation (VA) secondary to a reduction in upper airway dead space (VD) or 2) is dependent on an upper airway sensory mechanism. Three normal and three chronic CBD ponies were studied while they were breathing room air and at 14, 28, and 42 Torr PICO2. While the ponies were breathing room air, physiological VD was 483 and 255 ml during nares breathing (NBr) and tracheostomy breathing (TBr), respectively. However, at elevated PICO2, mixed expired PCO2 often exceeded PaCO2; thus we were unable to calculate physiological VD using the Bohr equation. At all PICO2 in normal ponies, PaCO2 was approximately 0.3 Torr greater during NBr than during TBr (P less than 0.05). In CBD ponies this NBr-TBr difference was only evident while breathing room air and at 28 Torr PICO2. At each elevated PICO2 during both NBr and TBr, the increase in PaCO2 above control was always less in CBD ponies than in normal ponies (P less than 0.01). The VE-PaCO2, f-PaCO2, and tidal volume-PaCO2 relationships did not differ between NBr and TBr (P greater than 0.10) nor did they differ between normal and CBD ponies (P greater than 0.10). We conclude that the attenuated increase in PaCO2 during CO2 inhalation after CBD is not due to a relative increase in VA secondary to reducing upper airway VD.(ABSTRACT TRUNCATED AT 250 WORDS)